Ku70 Corrupts DNA Repair in the Absence of the Fanconi Anemia Pathway

Author:

Pace Paul1,Mosedale Georgina2,Hodskinson Michael R.1,Rosado Ivan V.1,Sivasubramaniam Meera1,Patel Ketan J.1

Affiliation:

1. MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.

2. Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK.

Abstract

Righting Repair Pathways The genetic disease Fanconi anemia (FA) results from mutations in a series of genes involved in a DNA repair pathway that helps process the damage caused by erroneous chemical cross-links between the two strands of the DNA double helix. The double-stranded breaks in DNA that arise from such cross-links can be repaired in an error-free manner or through an error-prone repair pathway. Pace et al. (p. 219 , published online 10 June) show that the FA pathway can drive repair through the error-free pathway. The FA FANCC gene shows a genetic interaction with a component of the error-prone repair pathway, Ku70, inhibiting its action and thereby promoting the error-free pathway.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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